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Post traumatic Stress Disorder PTSD Overview


									Posttraumatic syndrome

   Surakrant Yutthakasemsunt , M.D
     Khonkaen Regional Hospital
         Khonkaen ,Thailand
             23 June 2006
• Wastebasket term
• No unique clinical diagnostic criteria
• Controversy in etiological details
• Inconsistency clinical presentation
• Limit of study methodological problems
          Related Terms
•   Posttraumatic syndrome:PTS
•   Posttraumatic stress disorder:PTSD
•   Posttraumatic stress syndrome
•   Posttraumatic neck syndrome
•   Post-Concussive Syndrome:PCS
  Posttraumatic stress disorder
• Shell shock
• Battle fatigue
• Accident neurosis
• Post rape syndrome
Neurobiological Changes after TBI
– cortical contusions (mostly in severe TBI)
   • results in a loss of function served by that area

– white matter lesions
   • results in interruption of information processing between cortical

– diffuse axonal injury
   • results in slowed and inefficient information processing
   • disproportionately affects glutamatergic and cholinergic projections
       – results in problems with attention, memory, and various aspects of
         frontally-mediated cognition (ie, working memory, executive function)
   • may affect serotonergic systems
   • dysfunction in these systems may secondarily affect the efficiency of
     function in dopaminergic or noradrenergic systems
             Clinical Features

• Somatic-organic or physical problems
• Psychosocial or neuropsychiatry
• Cognitive problems

Mixed and fluctuating symptom features over time
   especially neuropsychiatry problems
Patterns of Post-Concussive Symptoms
Filter Effects of CNS Injury
• What does depression look like in
  someone who is non-verbal?
• What does manic hyperactivity look
  like in someone with quadriplegia?
• How do hallucinations and delusions
  present in someone who cannot
  describe them?
 Vulnerability to Side Effects
• Neuropsychiatric patients show
  increased frequency & severity of side
  effects to most psychotropics

• Can manifest as worsening of
  neurological problems (tremor,
  cognition, slowing, etc.)
      Medications and Drugs
    Associated with Aggression
• Alcohol: intoxication and withdrawal
• Hypnotic and anxiolytics: intoxication and withdrawal
• Analgesics (narcotics): intoxication and withdrawal
• Steroids (prednisone, cortisone, and anabolic steroids)
• Antidepressants: especially during initial phases of Rx
• Amphetamines and cocaine
• Antipsychotics: secondary to akathisia
• Anticholinergic drugs: delirium
• Quinolone antibiotics?
     General Principles
• Drug Impact on Cognition
  • Memory – Benzodiazepines,
    antidepressants (anticholinergic effects)
  • Attention – Benzodiazepines,
  • Speed of Information Processing –
    Benzodiazepines, neuroleptics, others
• Thus the very areas most affected by TBI
 Neurotransmitter Dysfunction after TBI
• Many neurotransmitters are involved in the
  regulation of cognition, emotion, behavior, and
  physical/motor function
• Principal neurotransmitters in regulation of
  frontal and frontotemporal functions include:
  – dopamine
  – norepinephrine
  – serotonin
  – acetylcholine
  – glutamate
  – gamma-aminobutyric acid (GABA)
 Ways of Altering Synaptic
Content of Neurotransmitters
       Dopamine Agonists
• A variety of agonists have been
  shown effective in animal models and
  are used clinically:
 –Methylphenidate (and other stimulants)
 Alpha-2-Adrenergic Agonists
• Infusion of A2A agonists improves
  WM function in primates and rodents
• guanfacine can improve WM in
  healthy individuals and may improve
  working memory after TBI
• Methylphenidate also has A2A
  agonist properties
   Cholinergic Augmentation
• Multiple studies demonstrate that cholinergic
  augmentation, generally using one of several
  cholinesterase inhibitors (e.g.,
  physostigmine, donepezil) can improve TBI-
  induced attention and memory deficits even
  in the late post-injury period (>1 year) in
  some TBI survivors
  – Taverni 1998; Whelan 2000; Cardenas 1994;
    Arciniegas 2001
     Prior to Treatment
• Accurate diagnosis is critical first step
• Know what you are treating before
• Are you treating the underlying
  disorder, or the comorbid
    Neuropsychological Battery (Some)
•   Orientation
     – Galvestone Orientation and Amnesia Test (GOAT)
•   Motor
     – Grooved Pegboard test
•   Attention,Cognition processing Speed
     – Wechsler Memory Scale-Revised Digit Span
     – Symbol Digit Modality Test
•   Visual Scanning,Analysis and Construction
     – Trailmaking Test
     – Boston Visual Discrimination Test
     – Wechsler Adult Intelligence Scale-Revised Block Design (WAIS-RBD)
•   Language
     – Control Oral Word Association Test (COWAT)
     – Multilingual Aphasia Examination Token Test
•   Memory
     – Wechsler Memory Scale-Revised Logical Memory
     – Rey Auditory Verbal Learning Test (RAVLT)
•   Problem Solving
     – Wisconsin Card Sorting Test
Why learn about medications?

• Improves care
• Improves your clinical skills
• Fosters participation in treatment
• Facilitates holistic approach to care
Psychopharmacological Approach

• Clarify/simplify current regimen

• Clarify critical target symptoms to treat

• Target specific symptoms
    Medication approaches

1. amelioration of specific somatic
   symptoms (e.g., headache,
   dizziness, sleep disturbances)
2. amelioration of psychobehavior
3. augmentation of cognition
Dosage Considerations

       Start lower

       Go slower

       Stop sooner
 Psychopharmacological Issues
• At present, there are no FDA approved
  treatments for cognitive, emotional, or
  behavioral impairment due to TBI
• Pharmacotherapies are generally modeled
  after those for patients with
  phenomenologically similar but
  etiologically distinct disorders (attention-
  deficit hyperactivity disorder, Alzheimer’s
  disease, etc.)
 Physical Symptoms After Concussion

• Headache                    • Fatigue
• Dizziness/ Dysequilibrium • Insomnia
• Aesthenia/ Weakness         • Anosmia
• Numbness/ Paresthesias • Photophobia
• Tinnitus/ Hearing ↓↓        • Blurred Vision
• Hypersensitivity to sound
     Post-concussive Headache
• Musculoskeletal
      – Upper Cervical Spine
• Neurogenic
      – Greater or Lesser Occipital Neuralgia
      – Scalp Neuroma from laceration or
• Vascular
      – Not very common (although more-so in
      --Overlap in receptive fields for upper cervical
  dorsal horns and spinal tract of trigeminal nerve
• “Dysautonomic”
Treatment of Post-Concussive Headache

• Musculoskeletal: NSAIDs, Amitryptiline, TP
 injection, PT, Manual Medicine
• Neurogenic: Injection, anticonvulsants,
 Amitryptiline, counter-stimulants, PT, TENS,
 Lidoderm patches
• Vascular: Abortive Rx, Preventative Rx
Post-Concussive “Dizziness”

        Postural Instability


       Vestibular Dysfunction
        (vertigo, nystagmus)
Post-Concussive Postural Instability

• Musculoskeletal
• Neurological
    – Visual
    – Proprioceptive
    – Vestibular
    – Integrative
Post-Concussive Vestibular Dysfunction

• Vertigo

• Gaze Instability

• Postural Control
  Post-concussive Vestibular Problems

• Benign Paroxysmal Positional Vertigo
• Central Positional (will not habituate)
• Cervicogenic (habituates)
• Perilymphatic fistula (bed rest, surgery)
• Endolymphatic hydrops
  – Betahistine, suppressants, surgery
• Unilateral Vestibular Loss
• Bilateral Vestibular loss
  – head and neck are rigid, gaze unstable
Evaluation of Post-Concussive Dizziness

• Neuro-otology consult
• Imaging
• Electronystagmography (ENG)
• Caloric/rotary testing
• Posturography
Treatment of Post-concussive Dizziness

• Physical Therapy
  – Habituation Exercises
  – “Liberatory” Exercises (BPPV)
  – Oculo-vestibular Exercises
• Behavioral
• Pharmacological
• Surgery
    Pharmacological Treatment of
     Post-Concussive Dizziness
•   Meclizine (Antivert)
•   Scopolamine (anticholinergics)
•   Benzodiazepines
•   Antihistamines
    – Loratadine ?

        All may impede “natural” recovery
           and/or effectiveness of therapy
  Emotional/Affective Symptoms
        After Concussion
• Irritability
• Lability /inappropriate emotions (Mood change)
• Depression
• Anxiety/agitation
• Decreased libido
• Impulsive
 Despite Diagnostic Challenges
• When behaviors change:
  – New behaviors
  – Change in frequency and intensity of previous

• Have a high index of suspicion for the common
 psychiatric disorders
Common Behavioral Syndromes
    in the Injured Brain
• Depressive Syndromes
• Dyscontrol Syndromes
• Attention Deficit Syndromes
• Sleep Disorders
• Psychotic Syndromes
Psychiatric Disorders and TBI
• Disorders of thought content and thought
  process complicate recovery from TBI
• Psychotic syndromes occur at rates greater
  than those in general population
• Injury severity positively correlated with risk
• Even in absence of formal criteria,many with
  TBI have psychotic symptoms
 Other Links to Psychosis
  – resembles delirium in many respects
  – Restlessness, fluctuating level of consciousness,
  – Hallucinations and delusions occur frequently
• Mood Disorders
  – Depression
  – Mania
• Seizure Disorders
      Aggression and TBI
• Acute phase: 35% - 96% of patients exhibit
  agitated behaviors
  – 89 patients assessed during the first six months
    after TBI, aggressive behavior found in 33.7% of
    TBI patients, compared to 11.5% of patients with
    multiple trauma but without TBI (Tateno et al)
• Recovery phase: 31% - 71% of patients with
  severe TBI and 5% - 70% of patients with mild
  TBI are agitated or irritable
• Irritability increases with more TBI’s
   Characteristics of Aggression
             After TBI
• Reactive: Triggered by modest or trivial stimuli
• Nonreflective: Usually does not involve
  premeditation or planning
• Nonpurposeful: Aggression serves no obvious long-
  term aims or goals
• Explosive: Buildup is NOT gradual
• Periodic: Brief outbursts of rage and aggression,
  punctuated by long periods of relative calm
• Ego-dystonic: After outbursts, patients are upset,
  concerned, and/or embarrassed, as opposed to
  blaming others or justifying behavior
Neuropathology of Aggression
• Hypothalamus
  Orchestrates neuroendocrine response to sympathetic arousal
  Monitors internal status
• Limbic system
     Activates and/or suppresses hypothalamus
     Input from neocortex
  Temporal cortex
     Associated with aggression on both ictal and interictal
• Frontal neocortex
  Modulates limbic and hypothalamic activity
  Associated with social and judgment aspects of aggression
    Factors Associated with
    Agitation in Brain Injury
    Adverse                     Aggression as
                  Illness       direct effect of
  Environment                    Brain Injury

Psychosis                         Depression

     Anxiety                Sundowning

 “Past” Treatment of Agitation
• Agitation often treated non-specifically
  with sedatives
  –Should target underlying causes
• No medication is approved by the FDA for
  agitation or aggression
  –May reflect inconsistent concepts and
Approach to Dyscontrol Syndromes

• Consider if due to:
  –Environmental factors
• If so, treat accordingly
    Evaluation of Cognitive and
      Emotional Symptoms
•   Imaging (not usually very helpful)
•   Neuropsychological Assessment
•   Detailed past history
•   Differential etiologies
    – Medications
    – Concurrent illness
    – Sleep disorders
Treatment of Post-Concussive
Affective/Emotional Problems
• Correct sleep disturbances
• Counseling Pharmacological
 – SSRI’s
 – Anticonvulsants (valproate, carbamazepine)
 – Propranolol
 – Psychostimulants
 – Atypical antipsychotics ?
Approach to Depression
• Trials of
  – SSRI
  –second SSRI
  –Low dose Desipramine or Bupropion
• Other
   Approach to Mania
• Valproic Acid
• Lithium
• Combination approaches
• Newer anticonvulsants
Approach to Dyscontrol
• If not due to other conditions:
   –Beta blockers
   –Calcium channel blockers
    Nonpharmacological Approach
•   Modify environment
•   Optimize stimulation
•   Use consistent routines
•   Assess/adapt to aggravating factors
•   Behavior management principles
•   Education
•   Support of patient and caregivers
   Flow Chart for Management
         of Aggression
   Employ nonpharmacologic
          principles                            Continue treatment as appropriate
                                         No       Identify ,most prominent neurobehavioral sx cluster
                                                                 match to relevant class

Depressive features     Manic features        Anxious features     Psychotic features    Aggression only

                                                                                         Empirical trials:
 Antidepressants                              Antidepressants                                • blockers
 Anticonvulsants       Anticonvulsants        Anticonvulsants        Antipsychotics        •Anticonvulsants
     Lithium                                    Anxiolytics                                •Antidepressants
                                                 Effective?               No
      Continue as appropriate
Consider eventual empirical withdrawal                           Adapted from Tariot et al; Ryan
Evidence Based Guidelines
• Workgroup for Neurobehavioral Consequences of TBI
   – sponsored by IBIA, CDC

• Reviewed current literature
• Class I - randomized, double-blind, placebo controlled
• Class II - data collected prospectively, or retrospective
  analyses based on clearly reliable data (observational,
  cohort, prevalence, case control)
• Class III (case reports, retrospective, etc)
 IBIA Evidence Based Review
        of NBC of TBI
• There were no Class I, or II studies found
  which addressed the treatment of
  psychotic syndromes
• Some Class III studies addressed these
  patient populations, many of these had
  such methodological flaws that they were
  not useable in establishing treatment
Class III – Psychotic Disorders
• Agents Used
  – Typical Antipsychotics
    • Chlorpromazine – Bamrah, 1991; n=1

  – Atypical Antipsychotics
    • Clozapine – Burke, 1999; n=1, Laddomada 1999; n=1
    • Olanzapine – Butler, 2000; n=1, Umansky, 2000; n=1
    • Risperidone – Schreiber, 1998; n=1
  Side Effects and Toxicity
• Overall no clear indication from the literature
  that those with TBI suffer increased frequency
  or severity of side effects, nor novel side
• Usual side effects do occur:
  – Akathisia on SSRI’s
  – Mania on TCA’s and SSRI’s
  – Sedation, weight gain, seizures on Clozapine
  – Cognitive impairment on Lithium
• Not clear that this is different from those who
  have not been injured
• The use of standard psychotropics for standard
  indications (i.e. antipsychotics for the treatment
  of psychosis) is an option for clinicians
  – Use same meds, but dose differently
  – Cannot match clinical profile to neurotransmitter
    profile of various meds
  – There is clearly a need for randomized clinical trials
    to assess the efficacy of antidepressants,
    anxiolytics, and antipsychotics in the treatment of
    brain-injured individuals
      Cognitive Symptoms
       After Concussion
• Concentration and Attention

• Memory and learning

• Easily distracted

• Slowed thinking ,planning and problem solving

• Language function & communication deficit
Treatment of Post-concussive
     Cognitive Problems
•   R/O contributing factors (Drug treatment)
•   Correct sleep disturbances
•   Counseling/Therapy
•   Pharmacological
    – Psychostimulants
    – Modafinil for excessive daytime fatigue
    – Antidepressants
    • SSRI’s
    • TCA’s (desipramine)
    • Buproprion
Approach to Cognitive Deficits
• Main target domains:
  – Memory : particularly working memory
  – Attention
  – Executive Functions
• Management
  – Baseline testing
  – Trial of DA, A2A, or Cholinergic agent
  – Methylphenidate – start 5 mg/day
  – Aricept - start 5 mg/d
  – Titrate up slowly as tolerated
  – Discontinue after 2 months if no improvement

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